TRT Clinic Revenue Loop
Testosterone converts to estrogen inside your body, and that conversion is not a side effect to be managed. It is part of how testosterone does its job.
Most men starting TRT understand the first half of that chain: testosterone goes up, some of it aromatizes into estrogen, estrogen goes up, clinic prescribes something called an aromatase inhibitor, which is a drug that blocks the enzyme responsible for that conversion. The estrogen comes down. That part most people follow.
What most people do not follow is what happens next, and understanding it changes how you see the entire protocol.
Your pituitary gland releases something called growth hormone, which is the signal your body sends out to trigger tissue growth and repair. But growth hormone does not do that work directly. It travels to your liver, and your liver converts it into something called IGF-1, which stands for insulin-like growth factor 1, and it is the actual molecule that tells your muscles, bones, and other tissues to grow and recover. Growth hormone is the message. IGF-1 is what carries it out.
That conversion in the liver, from growth hormone into IGF-1, requires estrogen to happen efficiently.
When you take testosterone, some of it aromatizes into estrogen, and that estrogen does something useful: it drives your liver to produce more IGF-1. That is part of why testosterone makes you feel better, recover faster, and build more muscle. It is not just the testosterone. It is what the testosterone becomes.
Now here is where the protocol breaks down.
A 2017 randomized controlled trial by Dias and colleagues tested this directly. Thirty-seven older men were given either transdermal testosterone gel or an aromatase inhibitor. The testosterone group saw their IGF-1 rise by 15.3 nanograms per milliliter. The group taking an aromatase inhibitor saw a rise of just 0.3 nanograms per milliliter. Same study design, same population. The difference between those two numbers is estrogen.
The aromatase inhibitor did exactly what it was supposed to do. It blocked estrogen. And by blocking estrogen, it blocked the liver's ability to convert growth hormone into IGF-1. The pathway simply could not run without the signal estrogen provides.
So a man starts testosterone, his estrogen rises, his clinic prescribes an AI, his estrogen crashes, and his IGF-1 production collapses with it. Then the clinic looks at his IGF-1 numbers and offers him IGF-1.
That is the loop.
The FDA-approved form of IGF-1 is called mecasermin, sold under the name Increlex, and it is approved for a condition called growth hormone insensitivity, sometimes called Laron syndrome, where the body cannot respond to growth hormone at all and therefore cannot produce IGF-1 regardless of hormone levels. That condition affects somewhere between 350 and 500 people worldwide. It is an orphan drug for a pediatric population with a rare genetic disorder. That is the intended patient.
A man on TRT whose clinic suppressed his estrogen is not that patient. His liver can produce IGF-1 perfectly well. It just needs estrogen to do it, and the clinic removed that estrogen.
The question of whether this is happening by accident or by design is worth sitting with. A 2020 survey by Butaney and colleagues found that 69.4 percent of 489 surveyed physicians were prescribing aromatase inhibitors for symptomatic elevated estrogen during TRT. Neither the Endocrine Society nor the American Urological Association recommends routine AI use for estradiol management in men on testosterone replacement. Both organizations published guidelines in 2018 saying exactly that. The practice is widespread and unsupported by the major clinical bodies that govern this area of medicine.
Some of those physicians likely do not know the mechanism. They see estrogen go up and they treat it as a problem, the way you would treat any abnormal lab value, without following the downstream consequences of the treatment. Others may understand the mechanism and prescribe the way they do anyway. The article cannot tell you which situation applies to your clinic. But the mechanism does not change based on the prescriber's intent.
If you are on testosterone and an aromatase inhibitor, get your IGF-1 checked. If your IGF-1 came back low and your clinic suggested supplementing it, ask what happened to your estrogen first. That question will tell you a great deal about whether the people managing your protocol understand what they are actually doing.
The broader point is this: estrogen in a man on TRT is not automatically an enemy. It is the downstream signal that drives IGF-1, protects bone density, supports cardiovascular function, and contributes to the recovery and body composition changes most men are seeking when they start testosterone in the first place. Managing it down to the floor does not optimize testosterone therapy. It dismantles it, and then charges you to replace what was removed.
The most expensive hormone protocol is one where someone sells you the problem and the solution in the same visit.
References
- **Dias JP et al.** "Effects of transdermal testosterone gel or an aromatase inhibitor on serum concentration and pulsatility of growth hormone in older men." *Metabolism*, 2017; 69:143-147. PMID: 28285644. RCT, 37 men aged 65+. Testosterone group: +15.3 ng/mL IGF-1. AI group: +0.3 ng/mL.
- **Butaney M et al.** "Treatment of estrogen levels in the management of hypogonadism: An anonymous survey of ISSM members." *Urology*, 2020; 141:68-74. PMID: 32045591. 69.4% of 489 surveyed physicians prescribed AIs for symptomatic elevated estrogen.
- **FDA Label (NDA 021839):** Increlex (mecasermin) approved for growth failure in children with severe primary IGF-1 deficiency. Orphan drug. Pediatric only.
- **Orphanet:** Laron syndrome affects approximately 350-500 individuals worldwide. Prevalence: 1-9 per 1,000,000.
- **AUA 2018 Guideline** (Mulhall JP et al., PMID: 29601923) and **Endocrine Society 2018** (Bhasin S et al., PMID: 29562364): Neither endorses routine AI use for estradiol management during TRT.
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